On the basis of the convergence of two independent lines of research, one morphologic and the other epidemiologic, we believe that we can develop a primate experimental model for preventing prematurity and its effects on many aspects of development, but especially the development of the brain. Etiological factors leading to prematurity will be further defined by continuing analysis of the pigtail monkey colony parents who produce our premature and full term subjects. The subjects will be selected from parents that are at either high or low risk for producing premature, low birth weight, and dead offspring. Prenatal stress will be applied to half of the pregnant females in each risk group. Neurohistologic, physical, physiological, and behavioral changes in development will be assessed in spontaneously born and caesarean-delivered full term and premature subjects studied for eight months after birth. These changes will be related to the parental risk factors, prenatal stress, and avoidance of mechanical birth trauma to identify specific causes and effects of prematurity in monkeys. Our long-term goal is to expand this model to selectively increase or decrease the incidence of prematurity, and to identify the quantitative behavioral, anatomical, physical, and physiological correlates of accompanying risk to neonatal and infantile death, mental retardation, and other developmental abnormalities.